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At least 19 recordsLinked to original sources
PubMed1979

[Muscle fiber hypertrophy and myocardial function of the left ventricle in patients with chronic volume stress and cardiomyopathy].

Left ventricular angiography and endomyocardial biopsy were performed in 10 patients with aortic insufficiency and in 10 patients with congestive cardiomyopathy. Muscle fibre diameter and interstitial fibrosis were determined. In aortic insufficiency the diameter of muscle fibres is highest in the endstage, while in congestive cardiomyopathy it is highest in the earliest stage.

Aortic Valve Insufficiency↗
PubMed1979

Changes of cardiac and skeletal muscle in pigs following transport stress. An electron microscopic study.

After lorry transport (60--120 min), fattening pigs (100--120 kg living weight) with clinical signs of exhaustion and acute circulation insufficiency showed acute ultrastructural damage to the myocard and the skeletal muscle. These represent the morphological equivalent of a stress induced cardiomyopathy and are to be counted among the stress myopathies of the pig. These changes may be caused particularly by the high lactate production of the predominantly glycolytically operating skeletal muscles and by the effects of cardial catecholamine release following transport stress. Attention is drawn to the model character of these changes for similar processes in humans.

Animals↗
PubMed1976

Myocardial blood flow in congestive and hypertrophic cardiomyopathy: relationship to peak wall stress and mean velocity of circumferential fiber shortening.

Myocardial blood flow/unit mass (MBF) and the determinants of myocardial oxygen consumption were measured in seven control subjects (group I) and 15 patients (pts) with cardiomyopathy (CM), group II (group IIa-congestive CM: 10 pts; group IIb-hypertrophic CM: 5 pts). In group I left ventricular (LV) MBF was 64 +/- 8 (SD) ml/100g-min; it was significantly lower in IIa (45 +/- 15 ml/100g-min, P less than 0.01) and IIb (39 +/- 7 ml/100g-min, P less than 0.01). However, calculated total LV flow (LV mass X MBF) was increased in the two CM groups. In nine CM pts, LV MBF increased in response to atrial pacing from 41 +/- 7 to 63 +/- 13 ml/100g-min. In group IIa, calculated peak wall stress was normal (4.39 +/hortening (MVcf) was significantly reduced (0.53 +/- 0;18 vs 1.26 +/- 0.12 circum/sec, P less than 0.01). In IIb, MVcf was normal but peak stress was significantly reduced (2.80 +/- 0.75 vs 4.51 +/- 1.10 dynes/cm2 X 10(5), P less than 0.05). Multiple regression analysis based on all pts yielded, MBF - 16.9 MVcf + 9.30 Stress + 0.26 Heart Rate - 26.4 (r=0.79). The data indicate that MBF is reduced in CM patients and the regression analysis suggests that MBF in these 22 pts with normal coronary arteriograms was determined largely by heart rate, peak stress, and ventricular performance.

Blood Flow Velocity↗
PubMed1978

Stress testing and working capacity in Chagas' cardiomyopathy.

The EKG response to exercise and the working capacity in a group of 70 patients with positive serology for Chagas' disease has been determined by stress testing on a bicycle-ergometer, in order to establish the usefulness of such a test in the early diagnosis of Chagas' cardiomyopathy. The exercise EKG provides information which cannot be obtained by other diagnostic procedures, since the stress test can induce or increase ventricular arrhythmia, and is particularly indicated in patients with Chagas' infection and the incipient forms of Chagas' cardiomyopathy. Measuring the working capacity is useful in order to establish the degree of functional impairment of each individual patient. After the application of oral digoxin, no significant increase of ventricular extrasystoles following exercise has been observed and the working capacity has improved in the majority of the studied cases with Chagas' cardiomyopathy.

Administration, Oral↗
PubMed1979

Myocardial contractile function in aortic stenosis as determined from the rate of stress development during isovolumic systole.

To assess myocardial contractile function in the chronically hypertrophied human left ventricle, the rate of stress development (dsigma/dt) as a function of developed stress (sigmaD) during isovolumic systole was examined. Results for eight patients with aortic stenosis were compared with those for seven subjects with normal left ventricular function and with those for five patients with idiopathic congestive cardiomyopathy. The rate of stress development (dsigma/dt) was nearly identical in patients with aortic stenosis and in normal subjects over a wide range of values of sigmaD but was significantly lower in patients with cardiomyopathy (P less than 0.01 versus control subjects and patients with aortic stenosis). Normal values for dsigma/dt held not only for patients with compensated pressure overload, but also for those patients with aortic stenosis with depressed left ventricular ejection fraction and overt congestive failure. Similar findings were obtained when the first derivative of left ventricular pressure (dP/dt) was examined as a function of developed left ventricular pressure in normal subjects and patients with aortic stenosis or cardiomyopathy. These results indicate that contractile function as characterized by the isovolumic rate of stress development is not necessarily impaired in chronic pressure overload hypertrophy.

Adult↗
PubMed2026

Distinct Effects of Rap1 Subtype A GTPase Deficiency on the Male Mouse Heart.

This study utilized a genetically engineered mouse model deficient in the small GTPase Rap1A (knockout/Rap1A-null) to understand the biological role of Rap1A in the heart. We examined differential protein expression in the left ventricle of Rap1A-null versus wild-type control C57BL/6 male mice (~5 months) using proteomics (nanoLC-MS/MS quantitative analysis), and in the whole heart of aged male mice (~16 months) using MAL-DI-TOF/TOF mass spectrometry. Additionally, we used an experimental model of acute cardiovascular stress and assessed the impact on heart tissue histology, gene expression and mortality risk. Rap1A-deficient hearts showed reduced size and reduced heart and left ventricular weights. Significantly reduced gene expression of extracellular matrix collagen type I and collagen type III was present under baseline and cardiovascular stress conditions. Assessment of the proteomic profile identified a crucial role of Rap1A in promoting healthy ventricular myocardium, as its deficiency exhibited increased impact on cytoskeletal, mitochondrial, metabolic and contractile protein expression in young and aged mice. In young Rap1A-deficient mice, overrepresentation analysis revealed markers myosin heavy chain 7 (β-MHC) and alpha-actinin-2 (α-actinin-2) associated with cardiomyopathies, and upon cardiac stress, showed mortality risk compared to controls. Altogether, these findings provide important insights into the role of Rap1A in cardiac structure and remodeling under basal and stress conditions in male mice.

Animals↗
PubMed1975

Cardiac hypertrophy and left ventricular end-diastolic stress.

Equatorial and longitudinal left ventricular wall stress were calculated at end-diastole in a group of 66 patients in sinus rhythm. Thirty-one patients had volume overload of the left ventricle: six with acute and 21 with chronic aortic incompetence, and four with chronic mitral incompetence. Another six patients had aortic stenosis and 25 had congestive cardiomyopathy. Four patients served as controls. Stress was calculated using a thick-walled ellipsoid model. In patients with volume overload and congestive cardiomyopathy, ventricular dilatation was accompanied by an appropriate increase in wall thickness so that the "stress conversion factor" (the factor relating pressure to stress) was normal and absolute stress depended on end-diastolic pressure. In pressure overload of the left ventricle (aortic stenosis), the increase in wall mass reduced the stress conversion factor so that aboslute fiber stress was normal. These data support the hypothesis that muscle fiber stress may be an important determinant of left ventricular hypertrophy.

Angiocardiography↗
PubMed1976

Hemodynamic studies on hypertrophied hearts in man.

A total of 31 patients were studied during cardiac catheterization. Hemodynamics in 9 cases with cardiac hypertrophy secondary to chronic volume load (MI, AI) and in 9 cases with cardiomyopathy were compared to those in 5 normal cases, 5 cases with MS and 5 cases with near normal left ventricle. A hypertrophied left ventricle had an enlarged cavity, an increased wall mass and an elevated systolic midwall tension. Peak systolic stress in left ventricular wall was normal in compensated patients with volume load, but below normal in compensated patients with cardiomyopathy. Peak systolic stress was elevated in decompensated patients either with regurgitation or with cardiomyopathy. The significance of this stress difference between volume over load and cardiomyopathy was discussed. Depressed pump function was observed in hypertrophied left ventricle especially in cardiomyopathy.

Adult↗
PubMed1978

Regional variations in calculated diastolic wall stress in rat left ventricle.

Principal radii of curvature and wall thickness were measured at the apex and three other loci on the free wall of the left ventricle in 16 rat hearts that had been fixed at end-diastolic pressure. The law of Laplace was applied to calculate the mean tensile stress at each locus. No significant variation was found among the nonapical loci, but apical stress was approximately twice the stress calculated for any nonapical locus. The higher stresses that must be borne by the apex may be a predisposing factor for apical aneurysm in certain cardiomyopathies such as Chagas' disease. These higher stresses may also help to promote apical aneurysms in patients with ischemic heart disease.

Animals↗
PubMed1978

Reduced left ventricular myocardial blood flow per unit mass in aortic stenosis.

Myocardial blood flow (MBF) per unit mass was measured in 10 patients (pts) with severe aortic stenosis (AS) and no significant aortic insufficiency, normal ejection fractions, and normal coronary arteriograms, using xenon-133 and a multiple crystal scintillation camera. MBF per unit mass was reduced in AS (53 +/- 13 mg/100g.min) in comparison to a group of seven normal control patients (69 +/- 12 ml/100g.min) (P less than 0.05). When normalized for heart rate. MBF remained depressed in aortic stenosis (0.65 +/- 0.11 ml/100 g.beat). MBF/beat was strongly related to peak left ventricular wall stress in both groups (r = 0.97). Individual values of MBF/beat were normalized for peak stress using an analysis of covarience; the adjusted mean values were 0.62 +/- 0.03 ml/100g.beat for the AS patients and 0.84 +/- 0.03 ml/100 g.beat for the control patients. There was no overlap between groups in adjusted MBF per beat. Values of MBF per beat and peak stress for a group of ten cardiomyopathy patients with depressed contractility were observed to fall close to the regression line for AS patients. The results suggest that variability in resting MBF in these AS patients is due primarily to differences in LV stress and that reduction in MBF per beat in this group may be due to reduced contractility.

Aortic Valve Stenosis↗
PubMed2026

Takotsubo Syndrome: The First Non-Acute Proteomic Analysis by Remote Dried Blood Microsampling.

Takotsubo syndrome (TTS) is an under-recognized form of acute-onset heart failure typically precipitated by stress. While recovery of cardiac function is described over the course of weeks, adverse outcomes after apparent recovery are increasingly recognized. However, the pathophysiology of non-acute manifestations remains poorly understood. We used mass-spectrometry-based discovery proteomics from remotely collected non-acute dried blood microsamples to perform a case-control study in 62 participants with a prior TTS episode (median of 2.24 years prior to sample collection) and 47 reference controls. We quantified 398 unique proteins, and found that agnostic clustering techniques showed separation between TTS and reference control samples. This represents the first proteomic characterization of non-acute TTS. Pathway analysis of the 52 differentially regulated proteins demonstrated enrichment of proteins involved in complement activation, nitric oxide signaling, and with antioxidant activity. These enriched pathways may be suggestive of a persistent cardiomyopathy resulting from or predisposing to TTS.

Humans↗
PubMed2025

Cardiac hypertrophy at the crossroads: Mechanistic insights and emerging multimodal therapeutic strategies.

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide, accounting for approximately 17.9 million deaths annually. Among their diverse manifestations, cardiac hypertrophy is a clinically significant condition that predisposes patients to heart failure, arrhythmias, and and sudden cardiac death. Clinically, hypertrophy can be classified into three forms: physiological (adaptive) hypertrophy, which supports cardiac performance and is reversible, pathological hypertrophy most often secondary to hypertension, valvular disease, hemodynamic stress, or sustained neurohumoral activation; and hypertrophic cardiomyopathy (HCM) represents a primary genetic disorder, most often caused by mutations in sarcomeric proteins. These distinct etiologies have important therapeutic implications, as they determine how efficiently pharmacological agents can target underlying mechanisms. Conventional pharmacological treatments are widely used in clinical practice, yet they provide limited reversal of established remodeling. This therapeutic gap has driven the development of innovative modalities such as RNA-based therapeutics, exosome-mediated interventions, stem cell-derived therapies, and genome-editing technologies, which aim to modulate maladaptive signaling and restore myocardial integrity. This review integrates clinical perspectives with mechanistic insights, delineating the drivers of pathological hypertrophy while evaluating both established therapies and emerging strategies that hold promise for precision cardiology and improved patient outcomes.

Humans↗
PubMed1978

Cardiac pharmacology and cardiomyopathy in Friedreich's ataxia.

Friedreich's ataxia is almost always associated with a cardiomyopathy. The cardiomyopathy and its attendant cardiopulmonary sequelae is the usual cause of death in this disease. The author reviews the known pharmacology of the heart, particularly as it applies to hypertrophic cardiomyopathy. The important role played by calcium and the possible role of taurine is stressed. Therapeutic possibilities are mentioned.

Adrenergic beta-Agonists↗
PubMed2025

Therapeutic Targeting of Decr1 Ameliorates Cardiomyopathy by Suppressing Mitochondrial Fatty Acid Oxidation in Diabetic Mice.

BACKGROUND: A significant increase in mitochondrial fatty acid oxidation (FAO) is now increasingly recognized as one of the metabolic alterations in diabetic cardiomyopathy (DCM). However, the molecular mechanisms underlying mitochondrial FAO impairment in DCM remain to be fully elucidated. METHODS: A type 2 diabetes (T2D) mouse model was established by a combination of high-fat diet (HFD) and streptozotocin (STZ) injection. Neonatal rat cardiomyocytes were treated with high glucose (HG) and palmitic acid (HP) to simulate diabetic cardiac injury. Gain- and loss-of-function approaches and RNA sequencing were utilized to investigate the role and mechanism of 2,4-dienoyl-CoA reductase 1 (Decr1) in DCM. RESULTS: By integrating the genomic data available in the Gene Expression Omnibus (GEO) with DCM rodents, we found that the transcriptional level of Decr1 was consistently upregulated in DCM (+255% for diabetic heart, p&#x2009;<&#x2009;0.0001; +281% for diabetic cells, p&#x2009;<&#x2009;0.0001). Cardiomyocytes-specific knockdown of Decr1 preserved cardiac function (+41% for EF, p&#x2009;<&#x2009;0.0001; +24% for FS, p&#x2009;=&#x2009;0.0052), inhibited cardiac hypertrophy (-34%, p&#x2009;<&#x2009;0.0001), fibrosis (-69%, p&#x2009;<&#x2009;0.0001), apoptosis (-56%, p&#x2009;<&#x2009;0.0001) and oxidative damage (-59%, p&#x2009;<&#x2009;0.0001) in DCM mice, while cardiomyocytes-specific overexpression of Decr1 aggravated DCM (-28% for EF, p&#x2009;=&#x2009;0.0347; -17% for FS, p&#x2009;=&#x2009;0.0014). Deletion of Decr1 prevented high glucose/palmitate (HG/HP)-induced hypertrophy (-22%, p&#x2009;=&#x2009;0.0006), mitochondrial dysfunction and apoptosis (-74%, p&#x2009;<&#x2009;0.0001) in cultured cardiomyocytes. Furthermore, RNA sequencing and functional analysis showed that Decr1 interacted with and upregulated pyruvate dehydrogenase kinase 4 (PDK4) in injured cardiomyocytes, and overexpression of PDK4 eliminated the benefits of Decr1 downregulation in DCM (-20% for EF, p&#x2009;=&#x2009;0.0071; -28% for FS, p&#x2009;=&#x2009;0.0022). Mechanistically, PDK4 acted as a kinase that induced phosphorylation and mitochondrial translocation of HDAC3. In the mitochondria, HDAC3 mediated the deacetylation of dehydrogenase trifunctional multienzyme complex &#x3b1; subunit (HADHA), contributing to excessive mitochondrial FAO and subsequent cardiac injury. From a screening of 256 natural products, we identified Atranorin and Kurarinone as potential inhibitors of Decr1, both demonstrating protective effects against DCM (Atranorin, +21% for EF, p&#x2009;=&#x2009;0.0134; +24% for FS, p&#x2009;=&#x2009;0.0006; Kurarinone, +20% for EF, p&#x2009;=&#x2009;0.0183; +27% for FS, p&#x2009;=&#x2009;0.0001). CONCLUSIONS: Our study delineates a molecular mechanism by which Decr1 potentiated higher mitochondrial lipid oxidation and cardiac damage by enhancing HADHA deacetylation through the PDK4/HDAC3 signalling pathway.

Animals↗